Abstract
Rheumatoid arthritis (RA) is a classic example of an autoimmune disorder, with chronic inflammation of the synovial membrane, and deterioration of cartilage and bone in the affected joints. The resultant pain, loss of function and permanent disability are also associated with increased morbidity and mortality. Although the symmetrical joint deformities are a predominant characteristic, the disease has many systemic features. Since the pivotal studies of Waaler [1], serum rheumatoid factor (RF) estimation has been a basic diagnostic aid, varying in popularity with changes in scientific trends and with considerable controversy over its significance. Yet 60 yr later it is still recommended as a prognostic indicator of disease activity and progression in the adult and juvenile forms of arthritis [2, 3]. Science moves in paradigms and for several decades T-lymphocytes have dominated the literature, but with the devotion of persistent researchers, such as Jo Edwards, the B-lymphocyte has moved again to centre stage in the aetiology and progression of RA. Moreover, a recent Delphi panel of senior rheumatologists concluded that the ‘highest value ever’ for serum RF levels was still the best laboratory indicator of disease severity [4].

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